Vulnerable plaque

Vulnerable plaque

A vulnerable plaque is an atheromatous plaque, an unstable collection of white blood cells (primarily macrophages) and lipids (including cholesterol) in the wall of an artery which is particularly prone to produce sudden major problems, such as a heart attack or stroke.

In many cases, a vulnerable plaque has a thin fibrous cap and a large and soft lipid pool underlying the cap. These characteristics together with the usual hemodynamic pulsating expansion during systole and elastic recoil contraction during diastole contribute to a high mechanical stress zone on the fibrous cap of the atheroma, making it prone to rupture. Increased hemodynamic stress correlates with increased rates of major cardiovascular events associated with exercise, especially exercise beyond levels the individual does routinely.

Generally an atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial lumen. Tearing of the cover is called "plaque rupture".

Repeated atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, which creates artery stenosis.


Researchers have found that inflammation in the arteries leads to the development of "soft" or vulnerable plaque, which when released aggressively promotes blood clotting.

Researchers now think that vulnerable plaque, see atherosclerosis is formed in the following way: [ [ Texas Heart Institute, Heart Information Center] ]
* Lipoprotein particles, which carry fats and cholesterol in the blood stream, are absorbed by the artery wall, past the endothelium lining, cholesterol is released and then oxidized. This process typically starts in childhood.
* Oxidized cholesterol is an irritant which causes the release of proteins (called cytokines).
* The cytokines make the artery wall sticky, which attracts immune-system white blood cells (specifically monocytes).
* The monocytes squeeze into the artery wall. Once inside, they transform into eating cells called macrophages and ingest the oxidized cholesterol droplets.
* The macrophages sometimes become so cholesterol and membrane laden that they die in place, releasing their fat laden membranes into the intracellular space. This attracts more macrophages.
* In some regions of increased macrophage activity, macrophage-induced-enzymes erode away the fibrous membrane beneath the endothelium so that the cover separating the plaque from blood flow in the lumen becomes thin and fragile.
* Mechanical stretching and contraction of the artery, with each heart beat, results in rupture of the thin covering membrane spewing clot-promoting plaque contents into the blood stream.

When this inflammation is combined with other stresses, such as high blood pressure (increased mechanical stretching and contraction of the arteries with each heart beat), it can cause the thin covering over the plaque to split, spilling the contents of the vulnerable plaque into the bloodstream. The sticky cytokines on the artery wall capture blood cells (mainly platelets) that accumulate at the site of injury. When these cells clump together, they form a clot, sometimes large enough to block the artery.

The most frequent cause of a cardiac event following rupture of a vulnerable plaque is blood clotting on top of the site of the ruptured plaque that blocks the lumen of the artery, thereby stopping blood flow to the tissues the artery supplies.

Upon rupture, atheroma tissue debris may spill into the blood stream; this debris is often too large (over 5 micrometers) to pass on through the capillaries downstream. In this, the usual situation, the debris obstruct smaller downstream branches of the artery resulting in temporary to permanent end artery/capillary closure with loss of blood supply to, and death of the previously supplied tissues. A severe case of this can be seen during angioplasty in the slow clearance of injected contrast down the artery lumen. This situation is often termed non-reflow.

Additionally, atheroma rupture may allow bleeding from the lumen into the inner tissue of the atheroma making the atheroma size suddenly increase and protrude into the lumen of the artery producing lumen narrowing or even total obstruction.


While a single ruptured plaque can be identified during autopsy as the cause of a coronary event, there is currently no way to identify a culprit lesion before it ruptures. Because artery walls typically enlarge in response to enlarging plaques, these plaques do not usually produce much stenosis of the artery lumen. Therefore, they are not detected by cardiac stress tests or angiography, the tests most commonly performed clinically with the goal of predicting susceptibility to future heart attack. Additionally, because these lesions do not produce significant stenoses, they are typically not considered "critical" and/or interventionable by interventional cardiologists, even though research indications they are the more important lesions for producing heart attacks.

The tests most commonly performed clinically with the goal of testing susceptibility to future heart attack include several medical research efforts, starting in the early to mid-1990s, using intravascular ultrasound IVUS), thermography,(near-infrared spectroscopy) careful clinical follow-up and other methods, to predict these lesions and the individuals most prone to future heart attacks. These efforts remain largely research with no useful clinical methods to date (2006).

Another approach to detecting and understanding plaque behavior, used in research and by a few clinicians, is to use ultrasound to non-invasively measure wall thickness (usually abbreviated IMT) in portions of larger arteries closest to the skin, such as the carotid or femoral arteries. While stability vs. vulnerability cannot be readily distinguished in this way, quantitative baseline measurements of the thickest portions of the arterial wall (locations with the most plaque accumulation). Documenting the IMT, location of each measurement and plaque size, a basis for tracking and partially verifying the effects of medical treatments on the progression, stability or potential regression of plaque, within a given individual over time, may be achieved.


Patients can lower their risk for vulnerable plaque rupture in the same ways that they can cut their heart attack risk: take aspirin, eat a proper diet, quit smoking, and begin an exercise program. Researchers also think that obesity and diabetes may be tied to high levels of C-reactive protein. [ [ Texas Heart Institute, Heart Information Center] ]


No clinically validated detection or treatment methods for vulnerable plaque exist currently. [Heart Disease and Stroke Statistics – 2006 update, American Heart Association.]

Current Research

Newer clinical trial results (2007), e.g. the COURAGE trial,cite journal |author=Boden WE, O'Rourke RA, Teo KK, "et al" |title=Optimal medical therapy with or without PCI for stable coronary disease |journal=N. Engl. J. Med. |volume=356 |issue=15 |pages=1503–16 |year=2007 |month=April |pmid=17387127 |doi=10.1056/NEJMoa070829 |url=] have demonstrated that aggressively treating some of the physiologic behavioral factors which promote atheromas with "optimal medical therapy" (not opening stenoses, per-se) produced the most effective results in terms of improving human survival and quality of life for those who have been identified as having already developed advanced cardiovascular disease with many vulnerable plaques.


Wikimedia Foundation. 2010.

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